Adiposity and interstitial lung abnormalities in community dwelling adults: the MESA cohort study.

Abstract Background Obesity is associated with restrictive ventilatory defects and faster rate of decline in forced vital capacity (FVC). This association is not exclusively mediated by mechanical factors and may reflect direct pulmonary injury by adipose-derived mediators. Research Question Is adipose tissue involved in the pathogenesis of interstitial lung disease (ILD)? Study Design and Methods We evaluated the association of CT measures of pericardial, abdominal visceral, and abdominal subcutaneous adipose tissue, with high attenuation areas (HAA) and interstitial lung abnormalities (ILA) in a large multi-center cohort study of community-dwelling adults, using multivariable-adjusted models. We secondarily evaluated the association of adipose depot size with FVC and biomarkers of obesity and inflammation. Results In fully adjusted models, every doubling in pericardial adipose tissue volume was associated with a 63.4-unit increase in HAA (95%CI 55.5-71.3), 20% increased odds of ILA (95%CI -2% to 50%), and a 5.5% decrease in percent-predicted FVC (95%CI -6.8% to -4.3%). Interleukin-6 levels accounted for 8% of the association between pericardial adipose tissue and HAA. Every doubling in visceral adipose tissue area was associated with a 41.5-unit increase in HAA (95%CI 28.3-54.7), 30% increased odds of ILA (95%CI -10% to 80%), and a 5.4% decrease in percent-predicted FVC (95%CI -6.6% to -4.3%). Interleukin-6 and leptin accounted for 17% and 18%, respectively, of the association between visceral adipose tissue and HAA. Interpretation Greater pericardial and abdominal visceral adipose tissue were associated with CT measures of early lung injury and lower FVC in a cohort of community-dwelling adults. Adipose tissue may represent a modifiable risk factor for ILD.